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2014 critical and urgent care PSAP

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Available continuing pharmacy education (CPE) credits: This PSAP book carries a possible 23.0 hours of BCPS
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Library of Congress Control Number: 2013956447
ISBN-13: 978-1-880401-01-9 (PSAP 2014 BOOK 1, Critical and Urgent Care)
Copyright ©2014 by the American College of Clinical Pharmacy. All rights reserved. This book is protected by
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Print versions are produced in the United States of America.
To cite PSAP properly:
Authors. Chapter name. In: Murphy JE, Lee MW, eds. Pharmacotherapy Self-Assessment Program, 2014 Book 1. Critical
and Urgent Care. Lenexa, KS: American College of Clinical Pharmacy, 2014:page range.

Table of Contents
Disclosure of Potential Conflicts of Interest
Continuing Pharmacy Education and Program Instructions

Critical and Urgent Care I Panel

Antibiotic Use in Patients Receiving CRRT


By Kathryn A. Connor, Pharm.D., BCPS, BCNSP
Learning Objectives
AKI Review
Baseline Knowledge Statements
Additional Readings
Abbreviations in This Chapter
Assessing Kidney Function
Management of AKI by CRRT
Drug Dosing Considerations
Self-Assessment Questions


Cardiac Arrest and Advanced
Cardiac Life Support
By Kristen A. Hesch, Pharm.D., BCPS
Learning Objectives
Baseline Knowledge Statements
Additional Readings
Abbreviations in this Chapter
Therapeutic Goals of ACLS
Clinical Characteristics
Emergency Care for Out-of-Hospital Cardiac Arrest
Role of the Pharmacist in ACLS
Drug Administration in Cardiac Arrest
Pharmacotherapy of VF/Pulseless VT
Pulseless Electrical Activity/Asystole
Post-Cardiac Arrest Care
Self-Assessment Questions


Off-label Drug Use in the ICU
By Ishaq Lat, Pharm.D., FCCM, FCCP, BCPS; and
Mitchell J. Daley, Pharm.D., BCPS

Acute Management of Burn Injury
By Claire V. Murphy, Pharm.D., BCPS
Learning Objectives
Baseline Knowledge Statements
Additional Readings
Abbreviations in This Chapter
Burn Classification
Metabolic Changes: the Ebb and Flow
Goals of Care
Metabolic Modulation
Venous Thromboembolism Prophylaxis
Sepsis and Infection
Pharmacokinetic and Pharmacodynamic Considerations
Self-Assessment Questions

PSAP 2014 • Critical and Urgent Care



Learning Objectives
Baseline Knowledge Statements
Additional Readings
Abbreviations in This Chapter
The Critical Care Patient
Examples of OLDU as Standard of Care
Type of OLDU in the ICU
Informed Consent for OLDU
Approach to OLDU in the Critically Ill
Self-Assessment Questions


Critical And Urgent Care II Panel


Thrombolytic Therapy in
Acute Ischemic Stroke
By Alexander J. Ansara, Pharm.D., BCPS; and
Dane Shiltz, Pharm.D., BCPS
Learning Objectives
Baseline Knowledge Statements
Additional Readings
Abbreviations in This Chapter
Pathophysiology of AIS
Thrombolytic Therapy
Quality Improvement Initiatives
Self-Assessment Questions


Table of Contents

Thrombotic and Bleeding Diatheses
in Critically Ill Patients

Care of the Kidney Transplant Recipient

By Wesley D. McMillian, Pharm.D., BCPS; and Joseph Aloi,
Pharm.D., BCPS

Learning Objectives
Baseline Knowledge Statements
Additional Readings
Abbreviations in This Chapter
Pretransplant Considerations
Immediate Postoperative Course
Early Posttransplant Course
Self-Assessment Questions

Learning Objectives
Baseline Knowledge Statements
Additional Readings
Abbreviations in This Chapter
Pathophysiology and Diagnosis
Patients Taking Novel OACs
Self-Assessment Questions

By Samir J. Patel, Pharm.D., BCPS


Severe Sepsis and Septic Shock
By Seth R. Bauer, Pharm.D., BCPS; and
Simon W. Lam, Pharm.D., BCPS

Infection in Critically Ill Patients
By Lisa Hall Zimmerman, Pharm.D., BCPS, BCNSP, FCCM; and
Janie Faris, Pharm.D., BCPS
Learning Objectives
Baseline Knowledge Statements
Additional Readings
Abbreviations in This Chapter
Clinical Evaluation
Disease States
Laboratory Diagnostic Strategies
Treatment Goals
Special Considerations
Self-Assessment Questions

Learning Objectives
Baseline Knowledge Statements
Additional Readings
Abbreviations in This Chapter
Quality Patient care
Quality Improvement with a Care Bundle
Self-Assessment Questions


By Victor Cohen, Pharm.D., BCPS, CGP; and
Samantha P. Jellinek-Cohen, Pharm.D., BCPS, CGP

By Kara L. Birrer, Pharm.D., BCPS

PSAP 2014 • Critical and Urgent Care


Stevens-Johnson Syndrome and
Toxic Epidermal Necrolysis

Pain, Agitation, and Delirium in the ICU
Learning Objectives
Baseline Knowledge Statements
Additional Reading
Abbreviations in This Chapter
Etiology, Pathophysiology, and Complications
Assessment and Treatment of Pain
Assessment and Treatment of Agitation
Assessment and Treatment of Delirium
Guideline Development
Drug Shortage Implications
Self-Assessment Questions
Critical And Urgent Care III Panel




Learning Objectives
Baseline Knowledge Statements
Additional Readings
Abbreviations in This Chapter
Clinical Evaluation
Self-Assessment Questions


Reference Ranges for Common Laboratory Testsa


Table of Contents

The start of a new edition of the Pharmacotherapy SelfAssessment Program (PSAP) is truly an exciting time. Our
mission remains the same today as for the first edition – to
provide evidence-based updates that will improve clinical
pharmacy practice and patient outcomes. However, to
accomplish this, PSAP must reflect the changes in practice
models, patient populations, and the overall health care
environment. This new edition introduces features and
formats designed to enhance information access while
accommodating individual learning styles.
PSAP remains a labor of love for the faculty panel chairs,
authors, and expert and professional reviewers, as well as
for us, the series editors. We contribute to this endeavor
because we are committed to the board certification
process and the national recognition of the expertise of
clinical pharmacists. We are also dedicated to sharing
the most up-to-date knowledge with our colleagues, and
driven to create opportunities for board certified clinicians
to participate in scholarly activity. The PSAP 2014–2015
releases are each carefully developed to identify clinically
relevant content, solid case-based examples, and fair but
challenging self-assessment questions that allow the tester
to demonstrate mastery of this important material.
For individual chapters, the focus continues to be
on significant new information rather than a review of

common knowledge about a topic. Authors incorporate the
latest national or international guidelines for management,
landmark clinical trials, and content that integrate
concepts of biostatistics, epidemiology, and health systems
to cover all identified domains for the pharmacotherapy
specialist. In response to feedback from PSAP users, many
authors have included case-based examples demonstrating
the application of concepts, a treatment algorithm or
decision tree, and a summative box with practice points
or pearls. On the first page of each chapter are listed the
baseline knowledge presumed on the part of the reader
and open-access literature resources that can provide this
knowledge, if needed. The process for developing selfassessment questions has been revised by carefully tying
the questions to objectives and material presented in the
books and incorporating a field-test process using panels
of specialists. It is our hope that these efforts will build on
and improve PSAP’s reputation as a quality professional
development tool for Board Certified Pharmacotherapy
We extend our heartfelt appreciation to all the faculty
panel chairs, authors, and reviewers for lending their time
and expertise to this new series; and to ACCP Publications
staff members for their ever-present willingness to help
and guide the development of this new series.
John E. Murphy and Mary Lee, series editors

PSAP 2014 • Critical and Urgent Care



Disclosure of Potential Conflicts of Interest
Consultancies: Theresa Allison (Arbor Pharmaceuticals);
Edward Grace (Presbyterian College IRB, St. Francis
Hospital, Society of Infectious Diseases Pharmacists);
Ishaq Lat (Critical Care Pharmacotherapy Trials
Network); Samir Patel (Biotest Pharmaceuticals);
Heather Johnson (Novartis); Kristina E. Ward (State
of Rhode Island Department of Health and Human
Services, Abacus Group);

Pharmacy and Health Sciences [spouse or significant
other]); Edward Grace (Florida Pharmacists
Association, Florida Society of Health System
Pharmacists, Self Regional Hospital); Stephanie
Nichols (Maine Occupational Therapists Association);
Dane Shiltz (Butler University); David Volles (Cubist
Nothing to Disclose: Joseph Aloi; Seth Bauer; Kathryn
Connor; Mitchell Daley; Patricia Jane Faris; Kristen
Hesch; Samantha Jellinek-Cohen; Simon Lam; Chigozie
Mason; William Z. Marcus; Melissa Marsinko; Joseph
Mazur; Wesley McMillian; Claire V. Murphy; Steven
Pass; Theresa Phung; Mirembe Reed; Michael Remkus;
Russel Roberts; Eimer M. Sanchez; Dustin Spencer;
Natasa Stevkovic; Said Sultan; Joseph Swanson; Mickala
Thompson; Alana Whittaker; Katy H. Wright; Lisa

Stock Ownership: Jeffrey Fong (Teva, Inc.); Heather
Johnson (Pfizer);
Royalties: Victor Cohen (ASHP);
Grants: Edward Grace (Department of Veterans Affairs);
Jeffrey Fong (Merck, Hospira); Kristina E. Ward (U.S.
Food and Drug Administration);
Honoraria: Alexander Ansara (Boehringer-Ingelheim
Pharmaceuticals, Bristol-Myers Squibb, Pfizer); Kara
Birrer (University of Florida College of Pharmacy);
Victor Cohen (Arnold and Marie Schwartz College of

ROLE OF BPS: The Board of Pharmacy Specialties (BPS) is an autonomous division of the American Pharmacists
Association (APhA). BPS is totally separate and distinct from ACCP. The Board, through its specialty councils,
is responsible for specialty examination content, administration, scoring, and all other aspects of its certification
programs. PSAP has been approved by BPS for use in BCPS recertification. Information about the BPS
recertification process is available at www.bpsweb.org/recertification/general.cfm.
Other questions regarding recertification should be directed to:
Board of Pharmacy Specialties
2215 Constitution Avenue NW
Washington, DC 20037
(202) 429-7591

PSAP 2014 • Critical and Urgent Care


Disclosure of Potential Conflicts of Interest

Continuing Pharmacy Education
and Program Instructions
Continuing Pharmacy Education Credit: The
American College of Clinical Pharmacy is accredited
by the Accreditation Council for Pharmacy Education
as a provider of continuing pharmacy education (CPE).
Purchasers who successfully complete all posttests for
PSAP 2014 Book 1 (Critical and Urgent Care) can earn
23.0 contact hours of continuing pharmacy education
credit. The universal activity numbers are: Critical and
Urgent Care I – 0217-0000-14-001-H01-P, 7.5 contact
hours; Critical and Urgent Care II – 0217-0000-14-002H01-P, 9.0 contact hours; and Critical and Urgent Care III
– 0217-0000-14-003-H01-P, 6.5 contact hours.

schedule new opportunities for credits from upcoming
ACCP professional development programs.
ACPE Continuing Pharmacy Education Credit: To
receive ACPE CPE credit for a PSAP module, a posttest
must be submitted within 3 years after the book’s release.
The appropriate CPE credit will be awarded for test scores
of 50% and greater. Credits will be back-dated to the date
of test submission. Statements of ACPE CPE credit
will be made available online within 45 days after the
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Posttest answers: The explained answers – with rationale
and supporting references – will be posted online 5 days
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You will also see a hyperlink to a PDF file with the correct
answers and explanations for that test.

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recertification CPE credit, a PSAP posttest must be
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Recertification credits earned from a passing score will be
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be directed to BPS at (202) 429-7591 or www.bpsweb.org.
The ACCP Recertification Dashboard is a free online tool
that can track recertification credits as they are earned and

PSAP 2014 • Critical and Urgent Care

Test Waivers: To receive electronic access to the
explained answers without submitting a posttest, click
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link to the online waiver form. By completing the waiver
form for a module, you waive the opportunity to receive
CPE credit for that module. After you submit a waiver for
a posttest, you will see a link to the PDF file that contains
the answers for the module you waived. Answers will be
available starting 5 days after the BCPS test deadline.


Program Instructions

Critical and Urgent Care I Panel
Series Editors:

Acute Management of Burn Injury

John E. Murphy, Pharm.D., FCCP, FASHP
Professor of Pharmacy Practice and Science
Associate Dean for Academic and Professional Affairs
University of Arizona College of Pharmacy
Tucson, Arizona

Claire V. Murphy, Pharm.D., BCPS
Specialty Practice Pharmacist – Burn/Surgical Critical Care
PGY2 Critical Care Residency Program Director
Department of Pharmacy
The Ohio State University Wexner Medical Center
Columbus, Ohio

Mary Wun-Len Lee, Pharm.D., FCCP, BCPS
Vice President and Chief Academic Officer
Pharmacy, Optometry, and Health Sciences Education
Midwestern University
Professor of Pharmacy Practice
Midwestern University
Chicago College of Pharmacy
Downers Grove, Illinois

Said M. Sultan, Pharm.D., BCPS
Clinical Specialist, Critical Care
Assistant Professor of Clinical Education
Department of Pharmacy
University of North Carolina Medical Center
University of North Carolina Eshelman School of
Chapel Hill, North Carolina

Faculty Panel Chair
Steven E. Pass, Pharm.D., BCPS, FCCM, FCCP
Associate Professor and Vice Chair for Residency Programs
Department of Pharmacy Practice
Texas Tech University Health Sciences Center School of
Dallas, Texas

Natasa Stevkovic, Pharm.D., BCPS
Clinical Pharmacist, Trauma – Burn Critical Care
CPE Education Coordinator
Department of Pharmacy
John H. Stroger, Jr. Hospital of Cook County
Chicago, Illinois

Cardiac Arrest and Advanced
Cardiac Life Support

Antibiotic Use in Patients
Receiving CRRT

Kristen A. Hesch, Pharm.D., BCPS
Assistant Professor
Department of Pharmacy Practice
Texas Tech University Health Sciences Center School of
Dallas, Texas

Kathryn A. Connor, Pharm.D., BCPS, BCNSP
Assistant Professor
Department of Pharmacy Practice
St. John Fisher College
Clinical Specialist
Critical Care
The University of Rochester Medical Center
Rochester, New York

William Z. Marcus, Pharm.D., BCPS
Pharmacy Clinical Specialist
Critical Care
Renown Regional Medical Center
Reno, Nevada


Mirembe Reed, Pharm.D., BCPS
Clinical Pharmacy Specialist in Cardiology
Pharmacy Department
Steward St. Elizabeth's Medical Center
Boston, Massachusetts
PSAP 2014 • Critical and Urgent Care

David F. Volles, Pharm.D., BCPS
Pharmacy Clinical Coordinator
Department of Pharmacy
University of Virginia Health System


Critical and Urgent Care I

Charlottesville, Virginia
Stephanie Nichols, Pharm.D., BCPS
Associate Professor
Department of Pharmacy Practice
Husson University School of Pharmacy
Bangor, Maine
Clinical Pharmacist- Psychiatry and Adult Medicine
Maine Medical Center
Portland, Maine

The American College of Clinical Pharmacy and the
authors thank the following individuals for their careful
review of the Critical and Urgent Care I chapters:
Julia Elenbaas, Pharm.D.
Anthem, Arizona
Emilie L. Karpiuk, Pharm.D., BCPS, BCOP
Oncology Pharmacist
Department of Pharmacy
Froedtert Hospital
Milwaukee, Wisconsin

Off-Label Drug Use in the ICU

Jeffrey T. Sherer, Pharm.D., MPH, BCPS
Clinical Associate Professor
Department of Clinical Sciences and Administration
University of Houston College of Pharmacy
Houston, Texas

Ishaq Lat, Pharm.D., BCPS, FCCP, FCCM
Clinical Coordinator – Critical Care Pharmacy
Department of Pharmacy Services
University of Chicago Medical Center
Chicago, Illinois

Dale Whitby, Pharm.D., BCPS
Managing Editor, Clinical Content
Elsevier/Gold Standard
Midlothian, Virginia

Mitchell J. Daley, Pharm.D., BCPS
Clinical Pharmacy Specialist, Critical Care
Department of Pharmacy
University Medical Center Brackenridge at Seton
Healthcare Family
Austin, Texas
Russel J. Roberts., Pharm.D.
Sr. Clinical Pharmacy Specialist
Department of Pharmacy
Tufts Medical Center
Boston, Massachusetts
Michael J. Remkus, Pharm.D., BCPS
Associate Professor
Department pf Pharmacy Practice
Husson University School of Pharmacy
Bangor, Maine
Clinical Practice Faculty
Department of Pharmacy
Maine General Medical Center
Augusta, Maine
Healthcare Advisor and Financial Manager
Importaciones J. Vivanco, S.A.C.
Lima, Peru
Theresa T. Phung, Pharm.D., BCPS
Lead Critical Care Pharmacist
Department of Pharmacy
Fountain Valley Regional Hospital and Medical Center
Fountain Valley, California
Clinical Assistant Professor of Pharmacy Practice
College of Pharmacy
Western University of Health Sciences
Pomona, California

PSAP 2014 • Critical and Urgent Care


Critical and Urgent Care I

Cardiac Arrest and
Advanced Cardiac Life Support
By Kristen A. Hesch, Pharm.D., BCPS
Reviewed by William Z. Marcus, Pharm.D., BCPS; and Mirembe Reed, Pharm.D., BCPS

Learning Objectives

5. Describe the role of hypothermia in post–cardiac arrest
care to optimize survival and neurologic recovery.
6. Justify a pharmacotherapy treatment plan for patients
with cardiac arrest arrhythmias, including monitoring to assess efficacy as well as potential adverse drug

1. Distinguish the major changes in the most recent
treatment guidelines for adult advanced cardiac life
support (ACLS) in emergency cardiovascular care.
2. Design a patient-specific treatment plan for the prevention of cardiac arrest based on the most recent
treatment guidelines.
3. Analyze the role of cardiopulmonary resuscitation
techniques, electrical devices, vascular access, drug
delivery, and drugs to improve the return of spontaneous circulation (ROSC) and survival in sudden
cardiac arrest.
4. Design a pharmacotherapy treatment plan for the
individual patient with pulseless ventricular tachycardia, ventricular fibrillation, pulseless electrical
activity, or asystole.

The 2010 publication of the International Consensus on
Cardiopulmonary Resuscitation (CPR) and Emergency
Cardiovascular Care (ECC) Science with Treatment
Recommendations marked the 50th anniversary of modern CPR. In that half-century, hundreds of thousands of
lives worldwide have been saved by resuscitation research
and clinical translation of the fundamentals of early recognition and access to emergency medical care.

Baseline Knowledge Statements
Readers of this chapter are presumed to be familiar with the following:
■■ The care of critically ill patients in an intensive care unit
■■ The cardiac conduction system and action potentials
■■ Pathophysiology of cardiac arrhythmias
■■ Basic interpretation of the electrocardiogram
■■ Pharmacologic management of patients with pulseless ventricular arrhythmias, pulseless electrical activity, and
■■ The treatment algorithms for advanced cardiac life support by the American Heart Association
■■ Emergency systems that can effectively implement the chain of survival

Additional Readings
The following free resources are available for readers wishing for additional background information on this topic.
■■ Field JM, Hazinski MF, Sayre MR, et al. 2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care Science. Circulation. 2010;122:S640-S933.
■■ Mottram AR, Page RL. Advances in resuscitation. Circulation 2012;126:991-1002.
■■ Dager WE, Sanoski CA, Wiggins BS, et al. Pharmacotherapy considerations in advanced cardiac life support.
Pharmacotherapy 2006;26:1703-29.

PSAP 2014 • Critical and Urgent Care


Cardiac Arrest and Advanced Cardiac Life Support

process for assigning a class and strength to each intervention recommended from American College of Cardiology
Foundation (ACCF)/AHA collaboration in the 2010
Guidelines for CPR and ECC recommendations (Table
1-1). In the following discussion, strength of recommendation is indicated in parentheses.
This chapter reviews the important drug changes and
modifications in classes of recommendations in the 2010
CoSTR and AHA Guidelines for CPR and ECC in the
management of ventricular fibrillation (VF), pulseless
ventricular tachycardia (VT), pulseless electrical activity
(PEA), asystole, and bradyarrhythmias in adult patients.

Abbreviations in this Chapter

Advanced cardiac life support
Automatic external defibrillator
Basic life support
Coronary artery disease
Coronary perfusion pressure
Cardiopulmonary resuscitation
Emergency cardiovascular care
Emergency medical services
Public access defibrillator
Pulseless electrical activity
Return of spontaneous circulation
Sudden cardiac arrest
Transcutaneous pacemaker
Ventricular fibrillation
Ventricular tachycardia

Therapeutic Goals of ACLS
The ultimate goal in treating all forms of cardiac arrest
is long-term survival of a neurologically intact patient.
This is attained by accomplishing the following short-term
goals: (1) early CPR and defibrillation; (2) increased coronary perfusion pressure (CPP) and cerebral blood flow;
(3) ROSC; (4) survival to hospital admission; (5) stabilization of the patient; and (6) prevention of future SCA
episodes. The renewed emphasis on high-quality CPR
and attempted defibrillation for pulseless VT/VF and
advances in post-cardiac arrest interventions are considered the basis for improvement in survival.
The majority of trials testing ALCS interventions preceded the renewed emphasis on CPR and post–cardiac
arrest care , leaving questions about the effect of combining medications on outcomes such as survival. Because
the rate of survival post-arrest is so low, a large number of
SCA patients are required to detect a difference in longterm survival in clinical trials. Hence, other surrogate end
points such as ROSC, survival to admission to the hospital, survival for 24 hours, and survival at discharge from
the hospital are examined in most research. The clinical validity in assessing these more short-term outcomes
rather than quality of life and long-term survival comes
into question when discussing quality pharmaceutical
In point of fact, all other ACLS therapies including
drugs have not been shown to increase the rate of survival to hospital discharge. An important concept for the
pharmacist to understand and acknowledge is that most
all pharmacotherapeutic interventions in ACLS are secondary to implementation of high-quality CPR and
defibrillation. Medications should only be administered
after these activities have been initiated, because there
are no data demonstrating that drug therapy significantly
improves long-term outcomes.
The only rhythm-specific therapy of VT/VF proved
to increase survival to hospital discharge is defibrillation
as an integral part of uninterrupted, high-quality CPR.
Attempts to establish vascular access, administer drug
therapy, and advanced airway placement should not cause
significant interruptions in CPR or delays in defibrillation.

The first CPR guidelines were published in 1966, but
the final step in out-of-hospital resuscitation, known as
advanced cardiac life support (ACLS), was not published
until the 1974 update. The multiple links in the ACLS
chain of survival include interventions to prevent and
treat sudden cardiac arrest (SCA) and improve outcomes
of patients who achieve return of spontaneous circulation (ROSC) after SCA. The ACLS interventions build on
the basic life support (BLS) fundamentals of immediate
recognition and activation of the emergency response system, early CPR, and rapid defibrillation to further increase
the likelihood of ROSC through the use of drug therapy,
advanced airway management, and physiologic monitoring. After ROSC, survival and neurologic outcome can
be improved with integrated post–cardiac arrest care.
Although there have been many important changes since
the first guidelines, there are still few data to suggest that
drugs improve overall survival in all cardiac arrests.
The International Liaison Committee on Resuscitation
(ILCOR) includes resuscitation experts from 30 countries who meet every 5 years to identify, update, and review
research relevant to CPR and ECC. The ILCOR international resuscitation guidelines were updated in 2010
and published as the International Consensus on CPR
and ECC Science with Treatment Recommendations
(CoSTR). The individual member organizations related
treatment guidelines to their countries needs in terms of
the following: (1) geographic, economic, system differences in practice; (2) availability of medical devices and
drugs; and (3) ease or difficulty of training.
As one of ILCOR’s member councils, the American
Heart Association (AHA) transformed the international
resuscitation CoSTR into the 2010 AHA Guidelines for
CPR and ECC to provide clinicians with an integrated
evidence-based approach to ECC, BLS, and ACLS in both
adults and children. The AHA writers used the systematic
PSAP 2014 • Critical and Urgent Care


Cardiac Arrest and Advanced Cardiac Life Support

Table 1-1. Applying AHA Classification of Recommendations and Level of Evidence


Class I
Benefit >>> Risk
Treatment should
be performed /

Class IIa
Benefit >> Risk
Additional studies
with focused
objectives needed
It is reasonable to
perform procedure/
administer treatment

Class IIb
Class III
Benefit ≥ Risk
Risk ≥ Benefit
Additional Studies
Procedure/ Treatment
with broad objectives
should NOT
needed; additional
be performed /
registry data would
be helpful
because it is not
Procedure/ Treatment
helpful and may be
may be considered

Level A
Multiple populations
Data derived
from multiple
clinical trials or

Recommendation in
that procedure or
favor of treatment
treatment is useful/
or procedure being
Sufficient evidence
Some conflicting
from multiple
randomized trials or
from multiple
randomized trials or

less well established
Greater conflicting
from multiple
randomized trials or

that procedure or
treatment is not
useful/effective and
may be harmful
Sufficient evidence
from multiple
randomized trials or

Level B
Limited populations
Data derived
from single
randomized trial
or nonrandomized

that procedure or
treatment is useful/
Evidence from single
randomized trial
or nonrandomized

Recommendation in
favor of treatment
or procedure being
Some conflicting
evidence from single
randomized trial or

less well established
Greater conflicting
evidence from single
randomized trial
or nonrandomized

that procedure or
treatment is not
useful/effective and
may be harmful
Evidence from single
randomized trial
or nonrandomized

Level C
Very limited
Only consensus
opinion of experts,
case studies, or
standard of care

that procedure or
treatment is useful/
Only expert opinion,
case studies, or
standard of care

Recommendation in
favor of treatment
or procedure being
Only diverging expert
opinion, case
studies, or standard
of care

that procedure or
less well established
treatment is not
Only diverging expert
useful/effective and
opinion, case studies,
may be harmful
or standard of care
Only expert opinion,
case studies, or
standard of care

In addition, the exact timing of drug administration has
not been firmly established and is dependent on the establishment of vascular access, advanced airway placement,
and the number of properly trained providers present.
Given the lack of effective drug therapy, a focus of the
management of all SCA will be to accurately diagnose and
treat the underlying cause(s), focusing on the “Hs” and
“Ts” to identify, reverse, and treat any factor that may have
caused the arrest or may be complicating the resuscitative
effort (Table 1-2).

this circulatory collapse, the electrical activity of the heart
can be seen on a cardiac monitor as tachyarrhythmia, bradyarrhythmia, or asystole. Tachyarrhythmias include both VF
and pulseless or sustained VT, in which blood flow is inadequate and perfusion is insufficient to meet the body’s needs.
Ventricular fibrillation, or VT deteriorating to VF, is
the most common initial rhythm in SCA. After a variable
time spent in an initial tachyarrhythmic event (e.g., pulseless VT, VF), fibrillation may deteriorate to either asystole
or PEA. Asystolic events include severe bradyarrhythmias, during which the heart rate is too slow for adequate
tissue perfusion. The inability to generate an appropriate mechanical cardiac response is caused by either a
complete absence of electrical activity (asystole) or dissociation between abnormal spontaneous electrical activity
and mechanical function (pulseless electrical activity).

Clinical Characteristics
Cardiac arrest is an abrupt cessation of mechanical
function (evidenced by the loss of a pulse) and oxygen
delivery to vital organs such as the heart and brain. During

PSAP 2014 • Critical and Urgent Care


Cardiac Arrest and Advanced Cardiac Life Support

Table 1-2. Causes, Clues, and Interventions for Cardiac Arrest
Suspected Cause

Immediate Intervention

Rhythm May Be



Bolus fluids

Fast, narrow complex

Most common cause of PEA
All patients should receive fluid bolus


100% oxygen

Wide complex, slow

All patients should be adequately
ventilated hyperventilation, check ET


Wide complex, slow
(NaHCO3 1 mEq/kg IV x1)



Wide complex, slow







Toxins (overdose)

Alkalinize urine if
appropriate; CaCl if

Wide complex, slow
Question family members for possible
with overdose of TCAs,
OD in patient with no other clear cause
B-blockers, CCBs, digoxin of PEA

Tamponade (cardiac)

Needle aspiration of fluid

Wide complex, slow

Tension pneumothorax

Needle decompression;
chest tube

Consider in patients
with asthma

Thrombosis (cardiac;
myocardial infarction or
pulmonary; PE)







Sodium bicarbonate for hyperkalemia
(IIb/C); add D50W and insulin if ECG
changes are present


Fibrinolytics reasonable if presumed or
known PE (IIa/B)

ACLS = adult cardiac life support; CaCl = calcium chloride; CCB = calcium channel blockers; ET = endotracheal; IV = intravenous; IVP = intravenous push; K = potassium; NaHCO3 = sodium bicarbonate; OD = overdose; PE = pulmonary embolism; TCAs = tricyclic antidepressants.
Information from: Dager WE, Sanoski CA, Wiggins BA, et al. Pharmacotherapy Considerations in Advanced Cardiac Life Support.
Pharmacotherapy 2006;26:1703-29.

Coronary artery disease (CAD) is thought to account for
at least 80% of SCA in Western countries. The major cause of
SCA is atherosclerosis, which narrows coronary vessels over
time; this is followed by plaque rupture, platelet adhesion,
and an occlusive thrombus. The resulting ischemia and worsening myocardial instability likely induce pulseless VT and
VF. At autopsy, 81%–94% of victims of SCA have significant
CAD. Nearly one-half of people with CAD will experience
SCA as their first sign or symptom. Another 10%–15% of
SCA cases may be patients with systolic dysfunction and
non-ischemic cardiomyopathies possessing a myocardium
known to be vulnerable to ventricular arrhythmias.
When the myocardium is unable to respond to intrinsically generated electrical impulses (electromechanical
dissociation) or does not contract well enough to produce
an appreciable blood pressure, patients will exhibit cardiac
arrest as PEA. In contrast to pulseless VT or VF (likely from
CAD), PEA can result from several etiologies that impede

PSAP 2014 • Critical and Urgent Care

the myocardium from contracting effectively. Without resuscitative interventions, VF and PEA will deteriorate within
minutes into asystole, after which the prognosis is very poor.

Emergency Care for Out-ofHospital Cardiac Arrest
An estimated 50–55/100,000 persons suffer out-ofhospital cardiac arrest each year in the United States and
Canada and are treated by emergency medical services
(EMS); about 25% of these patients present with pulseless ventricular arrhythmias (Nichol 2008). The estimated
incidence of in-hospital SCA is 3–6/1000 admissions;
about 25% of these patients present with pulseless ventricular arrhythmias (Meanet 2010). In either setting, the time
elapsed between the critical rhythm event and the delivery of effective BLS and a ACLS components significantly
affects the patient outcome.


Cardiac Arrest and Advanced Cardiac Life Support

defibrillation within 3 to 5 minutes as the treatment of choice
for VF of short duration (I/A).
When a rhythm check reveals VF/VT and the defibrillator is charged, CPR should be paused to “clear” the patient
for a single shock. If oxygen has been placed on the patient,
it must be removed to prevent the possibility of combustion
secondary to the defibrillation attempt. Immediately after
the defibrillation attempt, CPR should be resumed without
a rhythm or pulse check and continued for 2 minutes. After
each 2-minute cycle, the provider giving chest compressions should switch to a different rescuer role to maintain
high-quality CPR and minimize fatigue. The management
of cardiac arrest with continuous high-quality CPR is summarized in Figure 1-1.

Defibrillation in VF/Pulseless VT
The single most effective treatment and most important
determinant for survival from VF arrest is establishing a

For the patient with VF, the chain of survival includes (1)
immediate recognition and activation, (2) early CPR, and
(3) rapid defibrillation. The likelihood of ROSC decreases
with each minute that passes without CPR; after about 30
minutes, the survival rate from SCA is 0%. In contrast, if
CPR is initiated within 5 minutes of arrest and defibrillation within 10 minutes, the rate of survival to hospital
discharge may be upwards of 37% (Berg 2008). If implemented in witnessed VF, the chain of survival can produce
almost 50% survival. In fact, only high-quality CPR and
defibrillation are proved to increase VF/pulseless VT survival to hospital discharge.

Continuous CPR

Continuous CPR

Basic Cardiac Life Support and Quality CPR
In most cases of witnessed and unwitnessed SCA, CPR
should be started by the first provider as the second provider
prepares the defibrillator/automatic external defibrillator
(AED). The BLS cardiac arrest algorithms emphasize the
importance of high-quality CPR,
defined as 100 chest compressions
per minute, at an adequate depth (2
inches), with complete chest recoil
Shout for Help / Activate Emergency
between compressions and miniResponse
mal interruptions.
Recent in-hospital observaStart CPR
tional studies found interruptions
Give oxygen
of chest compressions to averAttach monitor/defibrillator
age 24% to 57% of the total arrest
time. Incomplete chest wall recoil
2 minutes
Return of Spontaneous
is common, particularly when resCirculation (ROSC)
cuers are fatigued, and is associated
Rhythm If VF/VT
Post–cardiac arrest care
with higher intrathoracic pressures
and significantly decreased hemodynamics, including decreased
coronary perfusion, cardiac index,
Drug Therapy
myocardial blood flow, and cerebral
IV / IO Access
perfusion. The guidelines advocate
Epinephrine every 3 – 5 min
limiting interruptions (e.g., pulse
Amiodarone for refractory VF/VT
check) to 10 seconds or less to
Consider advanced airway
improve patient outcomes (Abella
Quantitative waveform capnography
2005) (IIa/ C).
Studies documenting the effect
Treat reversible causes
of bystander CPR show that surHs and Ts
vival rates from witnessed VF arrest
decrease by 7% to 10% per minute
without CPR. This is likely from
diminished microvascular blood
Monitor CPR Quality
flow, which is seen within 30 seconds of the onset of VF. Animal
models indicate that chest compressions begun within 1 minute of VF
Figure 1-1. Treatment of adult cardiac arrest.
arrest restore some microvascular
CPR = Cardiopulmonary Resuscitation; IO = intraosseous; IV = intravenous; ROSC
blood flow and improve survival. All
= Return of Spontaneous Circulation; VF = ventricular fibrillation; VT = ventricular
BLS providers should be trained to
provide immediate CPR and rapid
PSAP 2014 • Critical and Urgent Care


Cardiac Arrest and Advanced Cardiac Life Support

perfusing rhythm with defibrillation. Survival from VF may
be as high as 90% if defibrillation is initiated within 1 minute. However, it drops to about 50% at 5 minutes and 10%
at about 10 minutes. This is because each 1-minute delay
will decrease the probability of successful defibrillation
and increase the tendency of untreated VF to convert to
asystole, which carries a much poorer prognosis. Survival
rates are higher when the time to first defibrillation is minimized (I/B); the strength of recommendation decreases
with each subsequent defibrillation (IIb/B). The exact time
before VF converts to asystole is unknown. Other important interventions (e.g., intubation, intravenous access,

initiation of drugs) should be performed but should not
take precedence over quality CPR and defibrillation. The
management of VF/pulseless VT is summarized in Figure
To terminate VF with defibrillation, electrode pads are
placed on the patient’s exposed chest in an anterior-lateral position and a single shock is delivered (by a biphasic
defibrillator, if available) (I/B). The current from a biphasic defibrillator rapidly alternates from positive to negative
flow, as opposed to monophasic defibrillators, which delivers unidirectional current. Repeated, lower energy, biphasic,
fixed waveform shocks are equally or more effective than

Circulation: Start high quality, uninterrupted aCPR immediately
attach monitor when available and check rhythm
Airway: maintain patent airway
Breathing: give rescue breaths; give O2 when available

If pulseless VT/VF on rhythm check, give 1 shock by manual biphasic (120-200 J) or
monophasic defibrillator (360 J) and continue aCPR for 2 minutes; establish IV/IO access
If asystole of PEA activity on rhythm check, see Figure 1-3
If organized electrical activity on monitor with pulse, provide post-resuscitation care

Immediately resume aCPR for 2 minutes; check rhythm
If pulseless VT/VF on rhythm check, give 1 shock by manual biphasic, or monophasic
defibrillator & resume aCPR for 2 minutes; repeat every 2 minutes
If asystole of PEA activity on rhythm check, see Figure 1-3
Identify and treat possible reversible causes of cardiac arrest, see Table 1-2
If organized electrical activity on monitor with pulse, provide post-resuscitation care

Give vasopressors when IV/IO access available; Epinephrine 1 mg IV/IO every 3 – 5 minutes OR
Vasopressin 40 units IV/IO to replace first or second dose of epinephrine
Immediately resume aCPR for 2 minutes; check rhythm and repeat as above
Consider antiarrhythmic administration if patient remains in pulseless VT/VF
o First-line: amiodarone 300 mg IV/IO x1; repeat 150 mg IV/IO x1 in 3 – 5 minutes
o Alternate: lidocaine 1– 1.5 mg/kg IV x1, then 0.5-0.75 mg/kg IV (max dose 3 mg/kg total)
If torsades de pointes: magnesium 1– 2 g IV/IO
Figure 1-2. Defibrillation and pharmacotherapy of pulseless VT /VF.
Compression-ventilation ratio 30:0 at a compression rate ≥ 100/min or continuous compressions if advanced airway.
CPR = cardiopulmonary resuscitation; ECG = electrocardiogram; IO = intraosseous; IV = intravenous; J = joules; O2 = oxygen; PEA =
pulseless electrical activity; VF = ventricular fibrillation; VT ventricular tachycardia.

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Cardiac Arrest and Advanced Cardiac Life Support

higher energy, escalating, monophasic shocks (van Alem
2003). Use of a multimodal defibrillator in manual mode
for in-hospital cardiac arrest may reduce the interruptions
of CPR required for rhythm analysis when the automatic
mode is used. However, based on current evidence, this
may be offset by increased frequency of inappropriate defibrillation. No published trials have compared manual and
automatic defibrillation for in-hospital SCA; however,
AEDs may facilitate defibrillation at a goal of less than 3
minutes from collapse, especially in areas where staff have
no rhythm recognition skills or defibrillators are infrequently used (IIb/C).
When cardiac arrest occurs in the out-of-hospital setting, and more than 5 minutes of VF will occur before
EMS arrival, there is insufficient evidence that CPR will
affect overall outcomes. The placement of AEDs in public areas was supported by data from the Amiodarone for
Resuscitation after Out-of- hospital Cardiac Arrest due
to Ventricular Fibrillation (ARREST) trial (Kudenchuk
1999). In ARREST, 30% of the out-of-hospital SCAs
occurred in public places. Therefore, the programs to distribute AEDs into public areas, combined with community
awareness and education of CPR and AED use, was given
high priority by AHA and similar organizations.
Use of the AED requires no training and just five simple
steps: (1) power on, (2) attach electrode pads, (3) analyze
rhythm (performed by the machine), (4) clear the patient,
and (5) defibrillate the patient. The AEDs are programmed
to integrate CPR with defibrillation by delivering three consecutive shocks, pausing to allow 1 minute of CPR, then
delivering the next set of shocks. The patient who experiences ROSC is assessed for breathing and a pulse so that
appropriate support measures can be implemented.
Several large prospective randomized trials (known as
the Public Access Defibrillation [PAD] trials) evaluated the
effects of lay rescuer AED use. In PAD, researchers found
that implementing lay rescuer CPR plus early AED use can
increase survival to hospital discharge in out of hospital cardiac arrest (Hallstrom 2004). A more recent retrospective
review demonstrated that AED application before EMS
arrival doubled the survival rate from out-of-hospital VF
arrest (odds ratio [OR] 1.8) (Wiestfield 2010) To maximize
survival from out-of-hospital SCA, the AHA recommends
lay rescuer AED programs in locations where SCA is most
likely to occur and where responders are trained in CPR
and AED use simultaneously (IIa/B).

medications only play a secondary role in the ACLS effort,
the skilled pharmacist who is able to be one step ahead of
the team on the treatment algorithm is highly valued.
In a code situation, the costs of successful advanced
preparation (including wasted drugs) is of minimal concern. The pharmacist member of an in-house cardiac arrest
team should provide optimal medications at the correct
dose and frequency; assist by making recommendations;
provide compatibility information; and be well versed in
the rationale for ACLS medications, as well as the current
AHA class and level of evidence for recommendations.
Pharmacists with additional training in rhythm recognition
are able to prepare the appropriate drugs more quickly and
provide information related to the cardiac rhythm being
Pharmacists on multidisciplinary in-hospital cardiac
arrest teams or working in the hospital emergency department should gather pertinent data at the time of patient
arrival, including: (1) interventions performed; (2) what
drugs (e.g., dose, route, frequency) were given; and (3)
how the patient responded. A heightened awareness of
all administration times, doses, and concentrations for all
drugs given can help anticipate the appropriate next steps.
Direct communication with the EMS personnel, when possible, is best to confirm the drug administration record.
The EMS personnel are authorized to give certain drugs to
patients in the field; this is commonly done through a protocol or through direct contact with the nearest emergency
department. Typical drugs administered by EMS include
all ACLS drugs and potentially, more specialized agents,
such as thrombolytics for treating a ST-elevation myocardial infarction. Paramedics routinely performed ACLS
measures in many of the clinical trials evaluating vasopressin, epinephrine, and amiodarone.
In 2011, a practice opinion paper was prepared by a task
force of critical care clinical pharmacists including members of the ACCP Practice Research Network, the Society
of Critical Care Medicine Clinical Pharmacology and
Pharmacology Section, and the American Society of Health
Systems Pharmacists. The paper identified CPR response as
a required skill that should be documented and considered
“fundamental” for all levels of service by in-patient pharmacists, together with primary order-processing roles and
responsibilities (Dager 2011). To help ensure comfort on
the cardiac arrest team or in the emergency department
responding to CPR codes, the pharmacist should become
certified as an ACLS provider. Although course content
varies across the United States, the typical qualifications
to become ACLS certified include BLS certification and
successful completion of an AHA-sponsored ACLS certification course.

Role of the Pharmacist in ACLS
Each member of the multidisciplinary cardiac arrest team
should understand the skills, roles, and potential limitations
of the other team members to ensure that the code runs as
efficiently as possible. Although the properly trained pharmacist may perform any role on the team (including team
leader), the most befitting activities are likely related to
drug therapy and managing the crash cart drugs. Although

PSAP 2014 • Critical and Urgent Care

Drug Administration in Cardiac Arrest
Although time to drug treatment appears to have
importance during SCA, there is insufficient evidence to

Cardiac Arrest and Advanced Cardiac Life Support

specify the exact time or sequence in which drugs should
be administered. The pharmacist responding to a cardiac
arrest should accurately document all ACLS medications given including drug names, doses, administration
times, dosing intervals, total dose given, and the patient’s
response to drug therapy. The pharmacist may also work
closely with the person documenting code team activities
to ensure consistency and accuracy.
Although controversial, incompatibilities of intravenous and injectable drugs should not be a significant
concern during cardiac arrest. Because the primary
therapeutic goal is to resuscitate the patient as quickly
as possible, drug combinations are not exposed for a
prolonged time and therefore are not likely cause an immediate problem. One known incompatibility exception in
resuscitation medications is simultaneous administration
of calcium chloride and sodium bicarbonate (indicated in
a patient with significant hyperkalemia); this can cause
an immediate precipitate in the intravenous line and put
the patient at risk. Ideally, these two drugs should be given
through separate intravenous lines; if this is not possible,
a 20-mL fluid bolus should be administered after calcium
chloride to flush the line before administering sodium

Intravenous and Intraosseous Drug Delivery
A peripheral intravenous line is typically the easiest
to obtain during a resuscitation attempt. Although not
studied systematically, administering a 20-mL bolus of
intravenous fluid and elevating the patient’s arm for 20–30
seconds will use gravity to accelerate delivery to the central circulation.
As drugs are administered, high-quality CPR should be
continued to facilitate movement of the drug to the central circulation, which will take 1–2 minutes. Placement
of a central line (i.e., internal jugular or subclavian sites)
results in earlier and higher peak concentrations than
peripheral access. Central venous access, if already placed,
is the desired route of administration (IIb/C); however,
the administration of drugs and CPR should not be interrupted or delayed for the purpose of placing a central line.
Further, a newly placed central line is a relative contraindication to fibrinolytic therapy in patients with acute
coronary syndromes.
Alternatively, intraosseous cannulation enables drug
delivery similar to peripheral intravenous access at comparable doses. It is reasonable for providers to establish
intraosseous access if intravenous access is not readily
available. Although not extensively studied, most published data show that providers are able to establish
intraosseous access in all age groups efficiently, and that
this is a safe and effective alternative for fluid resuscitation, drug delivery, and blood sampling (Buck 2007; Lavis
2000). In the clinical setting, all ACLS drugs may be given
by the intraosseous without adverse effects during cardiac
arrest and ongoing CPR (IIa/C).
PSAP 2014 • Critical and Urgent Care

There are currently three devices with U.S. Food and
Drug Administration (FDA) label approval for insertion
of intraosseous access in adults. These devices are easier to
use than an intraosseous needle for cannulation and afford
a high success rate (about 80%). The most common adverse
effect reported with intraosseous access is extravasation
(12% of patients). Prolonged intraosseous access has
also produced reports of infectious complications (e.g.,
cellulitis, localized abscess formation, osteomyelitis), as
well as tibial fracture and compartment syndrome (Buck
2007). Box 1-1 lists drugs that can be administered by the
intraosseous route.

Endotracheal Drug Delivery
The endotracheal tube may be used to administer certain drugs such as epinephrine, vasopressin, lidocaine,
atropine, and naloxone. The absorption of resuscitation
drugs by the alveoli is rapid yet results in lower blood
concentrations than when the same dose is given intravascularly. If the endotracheal route is used in following SCA
resuscitation algorithms, each drug should be administered at 2–2.5 times the recommended intravenous dose
and diluted in 5–10 mL of sterile water or 0.9% normal
saline. Administration is repeated at the same interval as
for intravenous access.
To administer the drug down the endotracheal tube,
chest compressions are halted and the bag-mask unit
should be removed. After delivery, the bag-mask is rapidly replaced and the patient is given insufflations as
chest compressions resume. Data from two animal studies suggest that epinephrine administered endotracheally
may produce transient β2-adrenergic effects resulting
in vasodilation; this could be detrimental and potentially reduce ROSC. In a cohort of out-of-hospital cardiac
arrest adults, the administration of intravenous epinephrine and atropine resulted in a higher rate of ROSC and
5% higher survival to hospital discharge when compared
with endotracheal administration (Neimann 2003). Thus
intravenous or intraosseous routes of administration are
preferred in cardiac arrest and endotracheal administration should be reserved for cases in which intravenous or
intraosseous access cannot be established (IIb/B).

Pharmacotherapy of VF/Pulseless VT
The drugs listed in the ACLS algorithms can increase
rates of ROSC and survival to hospital admission but do
not affect long-term survival with a good neurologic outcome. One study randomized 1138 adults to intravenous
or no medications during management of out-of-hospital
cardiac arrest (Olasveengen 2009) The intravenous drug
group demonstrated significantly higher rates of ROSC
(40% vs. 25%) but there was no significant difference in
survival to hospital discharge (10.5% vs.9.2%) or survival
with favorable neurologic outcome (9.8% vs.8.1%). The

Cardiac Arrest and Advanced Cardiac Life Support

increased rates of ROSC with ACLS medications to be
translated into increased long-term survival. Defibrillation
is the mainstay of treatment for pulseless VF/VT as it is
the only effective means of re-establishing an organized,
perfusing rhythm. Some drugs may augment successful
defibrillation (vasopressors), and others may help prevent
further episodes of VF/VT (antiarrhythmics).

First-line Agents: Vasopressors
No placebo-controlled trials have shown administration
of vasopressors in SCA to increase the rate of neurologically intact survival to hospital discharge. However, there
is evidence that the use of vasopressors is associated with
an increased rate of ROSC. Based on current evidence,
when VF/pulseless VT persists after at least 1 defibrillation attempt and a 2-minute CPR period, a vasopressor
can be given with the primary goal of increasing myocardial blood flow during CPR and achieving ROSC (IIb/A).
Maintenance of adequate cerebral blood flow is important for neurologic recovery from SCA, although the
optimal cerebral perfusion pressure to maintain has not
been established. Properly performed CPR will preserve
blood flow in the short term and achieving ROSC will
reestablish blood flow; however, the time interval before
irreversible ischemia occurs is not known.
The most predictive factor for ROSC in patients not
responding to ventilation and defibrillation is an adequate
CPP. This is defined as the pressure gradient between the
aorta and the right atrium during the relaxation phase of
chest compression during CPR. The trough of the pressure waveform during this phase is known as the CPR
diastole because it is analogous to diastolic blood pressure.
The CPP therefore correlates with both myocardial blood
flow and ROSC during CPR.
Coronary blood flow (which depends on CPP) is vital
for oxygenation and defibrillation. Clinical monitoring of
CPP during a SCA situation is not practical and instead,
an arterial relaxation (“diastolic”) pressure measured
with a radial, brachial, or femoral artery catheter has been
proposed as a surrogate. Although it may be reasonable to
consider using diastolic pressure to monitor CPR quality as a means of optimization of parameters or giving a
vasopressor or both (IIb/C), a target arterial relaxation
pressure has not been established. One human study
found that all patients reaching the target CPP exhibited ROSC; however, none survived to hospital discharge
(Paradis 1990).
The endogenous release of vasoconstricting substances in response to SCA likely increases CPP but is not
sufficient to affect ROSC. Higher concentrations of circulating vasopressin levels were associated with increased
SCA survival, whereas epinephrine concentrations were
associated with decreased survival (Morris 1997). Both
drugs are known to increase CPP and are options for initial pharmacotherapy in VF/pulseless VT.

Box 1-1. Drugs that Can Be Administered by the
Intraosseous Route during Cardiac Emergencies
Cardiovascular Agents
Unfractionated Heparin
Central Nervous System Agents
Dextrose solutions
Lactated Ringers
Sodium Chloride
Calcium Chloride
Calcium Gluconate
Sodium Bicarbonate

study was not adequately powered to detect clinically
important differences in long-term outcomes.
A multicenter, controlled trial of more than 5000
patients found that the addition of ACLS interventions
including intravenous drugs in a previously optimized BLS
system with rapid defibrillation significantly increased the
rate of ROSC (18.0% vs.12.9%) and rate of hospital admission (14.6% vs.10.9%); however, no statistical difference
in survival to hospital discharge was seen (5.1% vs.5.0%)
(Steil 2004).
It is not clear whether optimized high-quality CPR
and advances in post–cardiac arrest care will enable the
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Cardiac Arrest and Advanced Cardiac Life Support

The systemic blood flow achieved by mechanical compression is 30% of the normal cardiac output. To maintain
cerebral, coronary, and overall perfusion, epinephrine
has traditionally been the vasopressor of choice in cardiac arrest. This agent stimulates α-adrenergic receptors
on the smooth muscle of peripheral vessels; the resulting
arterial vasoconstriction prevents arterial collapse and
increases coronary blood flow, cerebral blood flow, and
CPP. Additionally, α-adrenergic receptor activation may
promote defibrillation. The positive effects of epinephrine
may be negated by its beta receptor stimulation, which
can cause a dose-dependent increase in myocardial metabolic demands, impair oxygen delivery and consumption,
and increase lactate production in the post-resuscitation
No adequate randomized controlled trials have compared epinephrine with placebo in treatment of and
outcomes related to out-of-hospital cardiac arrest. A retrospective study comparing epinephrine with placebo in
sustained VF and PEA/asystole found improved ROSC
with epinephrine but no difference in survival (Herlitz
1995). There are also no vasopressors (norepinephrine,
phenylephrine) with proven survival benefit in SCA compared with epinephrine.
The optimal epinephrine dose is a main point of controversy. The rationale for higher doses is that worsening
acidosis diminishes tissue responsiveness to adrenergics.
Several studies compared high-dose (up to 10 mg) and
standard-dose (1 mg) epinephrine but found no added
benefit for most outcomes. A meta-analysis and other studies found improved ROSC with high-dose epinephrine,
but none demonstrated a survival benefit versus standarddose epinephrine in SCA (Vandycke 2000). Three studies
compared high-dose epinephrine (7–10 mg or 0.2 mg/
kg ) with standard-dose epinephrine (1 mg) and found
no difference in immediate survival, ROSC, successful
resuscitation, or survival to discharge from the hospital
(Woodhouse 1995; Brown 1992; Stiell 1992). In practice, the potential for post-resuscitation adverse effects
(e.g., myocardial dysfunction, instability, tachycardia and
hypertension from a hyperdynamic adrenergic state) have
eliminated routine use of higher doses. Especially vulnerable are patients with CAD who have impaired myocardial
perfusion at baseline; this can be further exacerbated by
excessive beta receptor stimulation with epinephrine.
In the largest study to date, 3327 out-of-hospital
patients with VF, PEA, or asystole were randomized to
high-dose (5 mg) versus standard-dose (1 mg) epinephrine given as repeated doses (up to 15 mg). The time to
drug administration was similar between the groups,
averaging about 20 minutes from the time of collapse.
Rate of ROSC and survival to hospital admission were significantly higher in the high-dose epinephrine group than
the standard-dose group, but neurologic outcome and
survival to discharge (secondary outcomes) were similar.

PSAP 2014 • Critical and Urgent Care

Interestingly, a subgroup analysis found that patients with
asystole as their presenting rhythm were more likely to
achieve ROSC and survive to hospital admission with
high-dose epinephrine. In contrast, patients with VF or
PEA as their initial rhythm had no difference in ROSC or
survival to admission between treatment groups. Survival
in all groups was very low, ranging from 1.1% in patients
receiving high-dose epinephrine and presenting with
asystole up to 11.3% in patients with VF receiving standard-dose epinephrine which may be caused by the long
delay in initial drug administration (Gueugniaud 1998).
In the same study, a subgroup comparison looked at 800
patients with defibrillation-refractory VF, PEA, or asystole administered either high-dose (15 mg), standard-dose
(1 mg) epinephrine or high-dose (11 mg) norepinephrine
at any time during ACLS resuscitation. No difference was
found between groups in rate of survival to discharge from
the hospital. The doses of epinephrine used were among
the highest studied; although found to be more effective
than standard dosing in achieving ROSC and survival to
hospital admission, they produced no effect on survival
(Gueugniaud 1998).
Epinephrine improves the rate of ROSC in cardiac
arrest, but no studies have demonstrated a difference in
survival. Overall, the higher rate of ROSC in these clinical
trials (30%–38%) is offset by the very poor rate of survival
to hospital discharge (2.3%–5%). It is therefore reasonable
to consider a 1-mg dose of intravenous or intraosseous
epinephrine administered every 3 to 5 minutes during
cardiac arrest (IIb/A), with higher doses considered only
in specific problems (e.g., β-blocker or calcium channel
blocker overdose, for endotracheal administration).

Vasopressin is a neuropeptide hormone that stimulates
V1 receptors on vascular smooth muscle cells, causing
intense vasoconstriction. It also stimulates V2 receptors
on the renal collecting duct, causing an antidiuretic effect.
In addition, the stimulation of V1 and V2 receptors exerts
a pro-coagulant effect that can increase the potential risk
of thrombosis.
Vasopressin began to be used in resuscitation guidelines in 2000 after animal data and small human studies
indicated its potential to increase CPP and coronary and
cerebral blood flow, thereby improving the rate of ROSC.
Compared with epinephrine, vasopressin has a more
gradual onset and more sustained effect (half-life, about
18 minutes). In theory, vasopressin could cause a sustained peripheral vasoconstriction, leading to increased
aortic pressure and negatively affecting post-ischemic
left ventricular function. It could also exacerbate regional
ischemia by impaired perfusion of a collateral-dependent
myocardium. However, neither adverse effect has been
seen in clinical use or in studies of patients with SCA.
Two randomized trials enrolled human cardiac arrest
victims to compare vasopressin (one dose, 40 units) with

Cardiac Arrest and Advanced Cardiac Life Support

epinephrine (1 mg); outcomes were found to be similar between patient groups (Gueugniaud 2008; Callaway
2006). Other investigators have examined the treatment
effect if either is given as the first-line option in VF/pulseless VT arrest. Three large, well-designed, randomized
controlled trials and one meta-analysis found no difference in ROSC, survival to discharge, or neurologic
outcome between vasopressin 40 units and epinephrine 1
mg as the first-line vasopressor in SCA.
The first of these RCTs assigned 1186 out-of-hospital arrest patients with similar baseline characteristics to
receive two injections 3 minutes apart of either 40 units
of vasopressin or 1 mg of epinephrine. If ROSC was not
restored, the patient was given an additional injection of
epinephrine and additional interventions such as sodium
bicarbonate, atropine, lidocaine, or amiodarone at the
discretion of the emergency department physician. No
significant difference between agents was seen in the
rates of hospital admission in patient with VF (46.2% vs.
43%) or patients with PEA (33.7% vs. 30.5%). However,
vasopressin demonstrated a significant advantage over
epinephrine in rates of hospital admission (29% vs. 20.3%)
and discharge (4.7% vs. 1.5%) for patients with asystole.
In the 732 patients who did not have ROSC after either
study drug, additional epinephrine significantly improved
rates of survival to hospital admission (25.7% vs. 16.4%)
and discharge (6.2% vs. 1.7%) in the vasopressin group,
but not in the epinephrine group. The authors concluded
that vasopressin followed by epinephrine may be more
effective than epinephrine alone in asystolic cardiac arrest
(Wenzel 2004).
On the basis of those data, a systematic review and
meta-analysis looked at five randomized controlled trials
comparing vasopressin and epinephrine in patients with
SCA (total n=1519). This analysis found no statistically
significant differences between vasopressin and epinephrine in regards to ROSC, death before hospital admission
or within 24 hours, death before hospital discharge, or
neurologic impairment in survivors. The subgroup analyses based on initial cardiac rhythm showed no statistically
significant difference between patients with VF, PEA,
or asystole, indicating that there is no clear advantage of
vasopressin over epinephrine (Aung 2005).
Two randomized, controlled trials also found no difference in outcomes when the combination of vasopressin
and epinephrine was compared with epinephrine alone in
patients with SCA. In the first trial, adults who received
more than one dose of epinephrine during CPR for out-ofhospital SCA were randomized to 40 units of vasopressin
(n=167) or placebo (n=158). The rate of ROSC and presence of pulses in the emergency department was similar
between vasopressin (31% vs. 30%) and placebo (19% vs.
23%). No subgroup of initial cardiac rhythm appeared to
be differentially affected, and after adjustment for other
clinical variables, no effect of vasopressin was evident.
Open-label vasopressin was administered after the study

PSAP 2014 • Critical and Urgent Care

drug for 19 placebo and 27 vasopressin patients, and no
difference in survival duration once admitted to the hospital was found (Callaway 2006).
In the second multicenter trial, out-of-hospital arrest
patients received either successive injections of a combination of vasopressin 40 units and epinephrine 1 mg
(n=1442) or epinephrine 1 mg and placebo (n=1452). The
patients were given the same combination of study drugs
if ROSC was not restored within 3 minutes. If ROSC
was still not restored within the following 3 minutes,
patients in both the combination therapy group and the
epinephrine-only group were given additional open-label
epinephrine at the discretion of the treating physician.
With similar baseline characteristics (excluding a higher
percentage of men in the combination therapy group),
no significant difference was seen between the combination-therapy and the epinephrine-only groups in survival
to hospital admission (20.7% vs. 21.3%) or in the secondary end points of ROSC (28.6% vs. 29.5%), survival to
hospital discharge (1.7% vs. 2.3%), good neurologic recovery (37.5% vs. 51.5%), and 1-year survival (1.3% vs. 2.1%)
(Gueugniaud 2008).
The effectiveness of repeated administration of vasopressin and epinephrine was studied in out-of-hospital
arrest patients receiving prolonged CPR immediately
after emergency department admission. Groups received
up to a maximum of four injections of either 40 units vasopressin (n = 137) or 1 mg epinephrine (n = 118). Patients
who received vasopressors before emergency department admission or suffered non-cardiogenic SCA were
excluded. No difference in the rates of ROSC (28.7% vs.
26.6%), 24-hour survival (16.9% vs. 20.3%), or survival to
hospital discharge (5.6% vs. 3.8%) was found. In subgroup
analyses, a significantly higher rate of ROSC was seen
with vasopressin than with epinephrine in patients who
had witnessed SCA (48.1% vs. 27.8%) or who received
bystander CPR (68.0% vs. 38.5%). However, when independent predictors of ROSC were calculated in the
subgroup analyses, vasopressin administration did not
affect the outcome (OR 0.87–0.28) (Mukoyama 2009).
In summary, controlled trials have not consistently
found the effects of vasopressin to differ from epinephrine
in patients with SCA. Therefore, a one-time, single dose
of vasopressin 40 units appears to be an equally effective
alternative to either the first or second dose of epinephrine (IIb/A). Repeated doses of vasopressin do not appear
to be beneficial and do not affect long-term survival and
therefore are not recommended.

Second-line Agents: Antiarrhythmics
Although antiarrhythmic agents are administered to
help prevent further episodes of VF/VT, there remains
no evidence that their routine dosing improves survival
to hospital discharge. The CoSTR and AHA Guidelines
recommend the use of a single antiarrhythmic agent if
possible, because the use of more than one may increase

Cardiac Arrest and Advanced Cardiac Life Support

potential adverse events after the patient is successfully
Amiodarone is the first-line antiarrhythmic agent. In
two blinded, randomized controlled trials, amiodarone
improved the rate of ROSC and increased short-term survival to hospital admission over placebo or lidocaine in
patients who experienced out-of-hospital VF/pulseless
VT cardiac arrest unresponsive to CPR, defibrillation,
and vasopressor therapy (IIb/B). Both the ARREST
and ALIVE trials used epinephrine as the initial vasopressor before amiodarone administration. The effects
of antiarrhythmics after vasopressin have not been studied; however, the current ACLS guidelines support this
If amiodarone is unavailable, lidocaine may be considered despite its relative inferiority to amiodarone in
improving rates of ROSC and survival to hospital admission (IIb/B). Magnesium sulfate should be considered
only for torsades de pointes associated with a long QT
interval (IIb/B). Procainamide is used as a last resort,
if at all, because of its potential for post-resuscitation
hypotension and a lack of efficacy data.

Amiodarone is useful for both atrial and ventricular tachyarrhythmias because of its multiple actions on
sodium, potassium, and calcium channels, as well as αand β-adrenergic blocking properties. First seen as useful
in the control of recurrent VT outside of the cardiac arrest
setting, amiodarone’s ability to improve rates of ROSC
and survival to hospital admission makes it the first-line
antiarrhythmic agent for VF or pulseless VT unresponsive
to CPR, defibrillation, and vasopressor therapy (IIb/B).
In 1999, the blinded, randomized controlled ARREST
trial enrolled 504 patients with out-of-hospital pulseless VT or VF arrest present after three precordial AED
shocks. The ARREST first responders (fire department
personnel) were trained in CPR/AED, and the second
responders (paramedics) were trained in ACLS. Patients
who were stable enough to be admitted to the emergency
department were intubated, received epinephrine 1 mg,
and enrolled in ARREST to be randomized to amiodarone
300 mg or placebo. On average, drugs were administered
20 minutes from the time of dispatch in both groups,
where 88% of patients were found in VF. Significantly
more amiodarone patients were admitted to the hospital with a spontaneous perfusing rhythm (regardless of
vasopressors), but still no difference in survival was seen
between groups. Because more patients were admitted to
the hospital, the cost of care with amiodarone was significantly higher than placebo (Kudenchuk 1999).
The Amiodarone versus Lidocaine in Ventricular fibrillation Evaluation (ALIVE) trial examined survival to
hospital discharge in patients with cardiac arrest and VF.
After three successive defibrillations, a single dose of epinephrine, and then another defibrillation, patients were

PSAP 2014 • Critical and Urgent Care

considered to have defibrillation-resistant VF and were
randomized to either amiodarone 5 mg/kg with a possible repeat dose of 2.5 mg/kg (n=179) or lidocaine 1.5
mg/kg with a repeat dose of 1.5 mg/kg if needed (n=165).
Significantly more patients survived to hospital admission
in the amiodarone group than in the lidocaine group (29%
vs. 15%) when drugs were administered within 24 minutes of initiation of resuscitative efforts. Interestingly, this
survival advantage was lost if the study drugs were administered later (Dorian 2002).
In ARREST, there was a higher incidence of bradycardia and hypotension in hemodynamically unstable
patients with VT. Although few human safety data exist,
a canine study administered a vasoconstrictor before
amiodarone to successfully prevent hypotension in termination of arrhythmias (Paiva 2003). Amiodarone’s
adverse effects on hemodynamics are attributed to vasoactive solvents (polysorbate 80 and benzyl alcohol) in the
intravenous formulation. An analysis of four prospective
trials in patients with VT (some hemodynamically unstable) found that amiodarone, administered without these
solvents, produced no more hypotension than lidocaine
(Somberg 2002). Additionally, slowing the rate of intravenous infusion also appears to minimize hypotension
in some patients. A premixed formulation of intravenous
amiodarone without these vasoactive solvents is now
approved for use in the United States, although the costeffectiveness of this formulation has not been established
in SCA.
The patient who is not successfully resuscitated by an
initial 300-mg bolus dose of amiodarone can receive supplemental 150-mg doses, although the efficacy of these
supplemental doses has not been studied. If ROSC is
achieved with amiodarone, an infusion should be started
at 1 mg/minute for 6 hours, followed by 0.5 mg/minute to
a maximal total dose of 2.2 g in 24 hours.

Before amiodarone, lidocaine was considered the
preferred antiarrhythmic for cardiac arrest. This longstanding and familiar agent was thought to have fewer
immediate side effects than other antiarrhythmics such
as procainamide. In animal studies, lidocaine’s ability
to increase the fibrillation threshold was seen to prevent
the emergence of VF immediately after acute myocardial
infarction. However, lidocaine has no proven short- or
long-term efficacy in cardiac arrest compared with placebo or epinephrine (Weaver 1990; Harrison 1981).
Only one older retrospective review linked lidocaine
with improved hospital admission rates in patients with
out-of-hospital VF arrest (Herlitz 1997). Most trial data
comparing lidocaine with either placebo or antiarrhythmic agents other than amiodarone are now considered
outdated. Therefore, there is a lack of adequate evidence
to recommend the use of lidocaine in patients with


Cardiac Arrest and Advanced Cardiac Life Support

refractory VT/VF, and the agent should only be considered if amiodarone is not available (IIb/B).
The recommended initial dose of lidocaine is 1–1.5
mg/kg; if pulseless VF or VT persists, additional doses of
0.5–0.75 mg/kg may be administered at 5- to 10-minute
intervals to a maximal dose of 3 mg/kg. After the ROSC, a
continuous infusion of 1–4 mg/minute is recommended,
with a reduction in the infusion rate to 1–2 mg/minute in
patients with impaired hepatic function, heart failure, or
low muscle mass. This reduction is meant to avoid neurologic adverse effects, mainly seizures. In the absence
of intravenous or intraosseous access, lidocaine can be
administered through an endotracheal tube at a dose of
2–4 mg/kg.

Few clinical trials have focused on the role of magnesium in cardiac arrest; therefore, the optimal dosing of
magnesium sulfate is based more on clinical experience.
Compared with other antiarrhythmic agents, magnesium
is nearly devoid of adverse effects with the exception of
hypotension, which can be managed after resuscitation.
In two observational studies, magnesium sulfate facilitated termination of torsades de pointes but was not
effective in terminating irregular/polymorphic VT in
patients with a normal QT interval (Manz 1991; Tzivoni
1988). For VF/pulseless VT cardiac arrest associated with
torsades de pointes, a 1–2 g bolus of magnesium sulfate
intravenous push diluted in 10 mL of 5% dextrose may be
administered (IIb/C). Three more recent randomized placebo-controlled trials did not identify a significant benefit
from use of magnesium among patients with VF arrest in
the prehospital, ICU, and emergency department settings
(Allegra 2001; Fatovich 1997; Thel 1997). Therefore, routine administration of magnesium sulfate in cardiac arrest
is not recommended (III/A) unless torsades de pointes is

Therapies Not Recommended During Cardiac Arrest
Sodium Bicarbonate
Historically, sodium bicarbonate (NaHCO3) has been
administered to correct acidosis in patients during circulatory collapse. Cardiac arrest results in low blood
flow and hypoxemia, precipitating the development of
anaerobic metabolism, lactic acidosis, local tissue acidosis, and ultimately acidemia. Acidosis impairs receptor
responsiveness to both endogenous and exogenously
administered adrenergic agents and may adversely affect
defibrillation, adrenergic responsiveness, ROSC, and
short-term survival. Because myocardial contractility
may be compromised by acidosis, NaHCO3 was though
to improve the responsiveness of the myocardium to the
effects of catecholamines. However, it is now recognized
that the routine use of buffers in cardiac arrest has no positive benefit and may have potential deleterious effects.

PSAP 2014 • Critical and Urgent Care

In two retrospective database reviews, bicarbonate use
was associated with increased ROSC, hospital admission, and survival to hospital discharge (Bar-Joseph 2005;
Weaver 1990) Since then, one prospective, randomized
controlled trial administered 250 mL of a buffer mixture
(NaHCO3, trometamol, disodium phosphate, and acetate)
or 0.9% sodium chloride to 502 patients who experienced
out-of-hospital VF and asystole arrest. The number of
patients with ROSC admitted to the ICU and discharged
alive did not differ between groups. A second prospective,
randomized controlled trial in 874 out-of-hospital arrest
patients administered a single empiric 1 mEq/kg dose
of bicarbonate or placebo after standard ACLS measures
(Vuknir 2006). There was no significant difference in survival between bicarbonate and placebo (7.4% vs. 6.7%),
and only if arrest was prolonged (i.e., greater than 15 minutes) was a trend toward improved outcome in survival
(32.8% vs.15.4%) observed with buffer administration.
Conversely, the use of NaHCO3 has many potential
disadvantages; the majority of available data associates
this agent with poorer outcomes compared with placebo (vanWalraven 1998; Roberts 1990; Delooz 1989;
Skovrov 1985). Exogenously administered NaHCO3 may
accumulate in the venous circulation, inducing extracellular alkalosis, exacerbating alkalemia, and inhibiting
the release of oxygen. In addition, the administration of
NaHCO3 during cardiac arrest can cause hyperosmolality
and hypernatremia; it may also produce carbon dioxide,
which freely diffuses into myocardial and cerebral tissue
and can paradoxically contribute to intracellular acidosis.
It has also been speculated that NaHCO3 may inactivate simultaneously administered catecholamines (Kette
1991; Graff 1985).
The routine use of NaHCO3 is strongly discouraged;
it should only be given when clearly indicated (irrespective of the systemic pH) in cardiac arrest patients (III/B).
According to the AHA Guidelines, base deficit should not
be completely corrected in order to minimize the risk of
iatrogenically induced alkalosis secondary to NaHCO3
administration. Buffers should only be used in clinical
situations as defined in Table 1-3. Whenever possible,
bicarbonate therapy should be guided by the bicarbonate concentration or calculated base deficit obtained from
arterial blood gas analysis.
In some specific resuscitation situations, NaHCO3
administration may be appropriate. Sodium bicarbonate
is always indicated in patients known to be hyperkalemic, with the typical initial dose being 1 mEq/kg, up to
a maximum of 50 mEq per dose. It may also be indicated
in patients who have known, pre-existing NaHCO3responsive acidosis; tricyclic antidepressant overdose;
intubation and mechanical ventilation with a prolonged
arrest interval; or who experience ROSC after a prolonged
arrest survival. Sodium bicarbonate is never indicated and
should not be used in patients with hypercarbic acidosis.


Cardiac Arrest and Advanced Cardiac Life Support

Table 1-3. 2010 AHA Guidelines ACLS Classes of Recommendations for Bicarbonate
Recommended Dose
Class IIb, LOE C
Cardiac arrest secondary to pre-existing
Sodium bicarbonate 50 mEq IV over 5 minutes
metabolic acidosis and severe hyperkalemia
as adjuvant IV therapy for cardiotoxicity in
addition to standard ACLS
Class IIb, LOE C
Cardiac arrest secondary to wide-complex
1 -2 mL/kg of sodium bicarbonate solution
tachycardia seen in cocaine poisoning/OD, (8.4%, 1 mEq/mL) IV as a bolus, repeated as
Vaughan-Williams class Ic antiarrhythmic
needed until hemodynamic stability is restored
agent OD, and TCA OD
and QRS duration is ≤120 ms
Class III, LOE B
Routine use in cardiac arrest
*clinical experience is greatly limited and
outcome studies are lacking
Potential ADEs
Severe alkalemia (pH > 7.55), hyperosmolality, severe hypernatremia (Na > 155 mEq/L),
hypoglycemia, intracellular acidosis (CO2), myocardial acidosis
ACLS = advanced cardiac life support; ADEs = adverse drug effects; AHA = American Heart Association; CO2 = carbon dioxide; IV = intravenous;
LOE = level of evidence; N/A = not applicable; Na = sodium; NaHCO3 = sodium bicarbonate; OD = overdose; TCA = tricyclic antidepressant.
Information from: Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: Cardiac Arrest in Special Situations: 2010 American Heart
Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122: S829-61

Other non–CO2-generating buffers (e.g., THAM) have
shown potential for minimizing some adverse effects of
NaHCO3 (Katz 2002; Sun 1996; Blecic 1991), but clinical experience is greatly limited and outcome studies are

Intravenous Fluids
There are no published human data directly comparing
outcomes with routine intravenous fluid administration
versus no fluids during CPR. Most of the human and animal studies to date have not included a control group.
Two animal studies showed that normothermic fluid infusion during CPR caused a decrease in CPP (Yannopoulos
2009; Ditchey 1984). Hypertonic and chilled fluids have
not shown a survival benefit in animal and human studies
(Bender 2007). Hypovolemic arrest should be suspected
when patients present with signs of circulatory shock
associated with extreme volume losses advancing to PEA.
Only in these settings should intravascular volume be
promptly restored.

Studies of patients with cardiac arrest have found variable effects of calcium on ROSC, and no clinical trial has
found a benefit on survival either in or out of hospital (vanWalraven 1998). Therefore the routine administration of
calcium for treatment of in-hospital and out-of-hospital
cardiac arrest is not recommended (III/B).
The recommended treatment of hyperkalemia with
electrocardiographic changes is 10% calcium chloride

PSAP 2014 • Critical and Urgent Care

500–1000 mg (5–10 mL) administered intravenously
over 2 to 5 minutes in sequence after dextrose and insulin to stabilize the myocardium and minimize the effects
of potassium on the myocyte. The 3-fold difference in
primary cation between calcium gluconate, which contains 4.65 mEq/g, and calcium chloride, which contains
13.6 mEq/g, makes chloride the preferred agent in ACLS.
However, if the patient lacks a central line access, calcium
gluconate is preferred to avoid phlebitis and skin irritation.

No prospective controlled clinical trials have examined
the use of atropine sulfate in asystole or bradycardic PEA
cardiac arrest. Data from low-quality clinical studies conflict in regard to the benefit of routine use of atropine in
cardiac arrest. Although included in previous versions of
the ACLS Guidelines, the 2010 update withdrew the recommendation for atropine use in VF/pulseless VT. There
is no evidence that atropine has detrimental effects; however, the evidence suggests that routine use of atropine
during PEA or asystole is unlikely to have a therapeutic
benefit, and it therefore should not be used in VF/pulseless VT (IIb/B)
Drug-induced VF/ Pulseless VT
Many drugs can induce VF/pulseless VT. Antiarrhythmics
all have proarrhythmic potential and typically cause a wide
complex VT with a prolonged QT interval, suggesting torsades de pointes. In addition, overdose of many other drug


Cardiac Arrest and Advanced Cardiac Life Support

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